Neurological complications of sepsis

Abstract

Purpose of review: Sepsis, defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, is a leading cause of hospital and ICU admission. The central and peripheral nervous system may be the first organ system to show signs of dysfunction, leading to clinical manifestations such as sepsis-associated encephalopathy (SAE) with delirium or coma and ICU-acquired weakness (ICUAW). In the current review, we want to highlight developing insights into the epidemiology, diagnosis, prognosis, and treatment of patients with SAE and ICUAW.

Recent findings: The diagnosis of neurological complications of sepsis remains clinical, although the use of electroencephalography and electromyography can support the diagnosis, especially in noncollaborative patients, and can help in defining disease severity. Moreover, recent studies suggest new insights into the long-term effects associated with SAE and ICUAW, highlighting the need for effective prevention and treatment.

Summary: In this manuscript, we provide an overview of recent insights and developments in the prevention, diagnosis, and treatment of patients with SAE and ICUAW.

Box 1

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FIGURE 1

Diagnostic flow-chart for ICU-acquired weakness (ICUAW), critical illness polyneuropathy, and critical illness myopathy. CMAP, compound muscle action potential; ENMG, electroneuromyography; MRCss, Medical Research Council Sum Score; PENT, peroneal nerve test.

FIGURE 2

Differential diagnosis of critical illness polyneuropathy and critical illness myopathy. Critical illness polyneuropathy (CIP) is an acute sensory–motor axonal neuropathy with reduced nerve action potential amplitude and normal conduction velocity. In demyelinating Guillain–Barré syndrome, the nerve action potential amplitude is normal while the nerve conduction velocity is reduced (right). Direct muscle stimulation (DMS) may distinguish CIP from CIM in noncollaborative patients. In CIM, the compound muscle action potentials (CMAPs) obtained through nerve stimulation (neCMAP) and direct muscle stimulation (dmCMAP) are proportionally reduced and their ratio is around 1. In CIP, the CMAP is reduced, while dmCMAP is normal and their ratio is small and around zero (left). However, CIP and CIM often coexist in patients with ICUAW (center). Adapted from Latronico et al. Curr Opin Crit Care 2005; 11: 126; and Kramer et al. Neurol Clin 2017; 35: 723. CIM, critical illness myopathy; CIP, critical illness polyneuropathy; CIPNM, critical illness polyneuromyopathy; CMAP, compound muscle action potential; CRIMYNE, critical illness myopathy and neuropathy; DMS, direct muscle stimulation; GBS, Guillain–Barré syndrome; ICUAW, ICU-acquired weakness.